Carotid Artery Dissection

No Results

No Results

processing….

Carotid artery dissection begins as a tear in one of the carotid arteries of the neck, which allows blood under arterial pressure to enter the wall of the artery and split its layers. The result is either an intramural hematoma or an aneurysmal dilatation, either of which can be a source of microemboli, with the latter also causing a mass effect on surrounding structures.

Carotid artery dissection is a significant cause of ischemic stroke in all age groups, but it occurs most frequently in the fifth decade of life and accounts for a much larger percentage of strokes in young patients. ^[1] Dissection of the internal carotid artery can occur intracranially or extracranially, with the latter being more frequent. Internal carotid artery dissection can be caused by major or minor trauma, or it can be spontaneous, in which case, genetic, familial, or heritable disorders are likely etiologies.

Although in practice, dissections are labeled spontaneous in the absence of major blunt or penetrating trauma, ^[2] when they are associated with minor mechanism trauma they may be caused or influenced by an underlying arteriopathy. ^[3] Patients can present in a variety of settings, such as a trauma bay with multiple traumatic injuries; a physician’s office with nonspecific head, neck, or face pain; or an emergency department (ED) with a partial Horner syndrome.

Sophisticated imaging techniques, which have improved over the past two decades, are required to confirm the presence of dissection. Most ischemic cerebral symptoms arise from thromboembolic events; therefore, early institution of antithrombotic treatment provides the best outcome. ^[4]

Once diagnosed and treated, patients with carotid artery dissection require regular follow-up and imaging studies of both carotid arteries. Healing usually takes 3-6 months, and the incidence of contralateral dissection is higher in these patients than in the general population. When the condition is diagnosed early, the prognosis is usually good. A high index of suspicion is required to make this difficult diagnosis.

For patient education resources, see the Brain & Nervous System Center, as well as Worst Headache of Your Life, Transient Ischemic Attack (TIA, Mini-Stroke), and Stroke.

Although the cause of internal carotid artery dissection remains elusive, mechanical forces (eg, trauma, blunt injury, and stretching) and underlying arteriopathies (eg, Ehlers-Danlos syndrome IV and other connective tissue disorders and aberrations), either alone or in combination, account for most of the pathophysiology. It is widely accepted that carotid artery dissection is a multifactorial disease. ^[5]

Carotid artery dissection begins as a tear in the tunica intima or directly within the tunica media (possibly originating from the vasa vasorum). ^[1] The blood dissects along the artery to create an intramural hematoma that leads to a thrombus, which can narrow the carotid artery lumen and become a nidus for distal embolization (see the image below). ^[2]

Sometimes, the dissection plane lies between the tunica media and the tunica adventitia, resulting in an aneurysmal outpouching of the arterial wall that may also become a source of distal emboli. Aneurysmal dilatation can also cause a mass effect on nearby structures such as sympathetic fibers and the lower cranial nerves. ^{[1, 2]} The dilatation resulting from an internal carotid artery dissection may be termed a true rather than a false aneurysm because the wall is composed of blood vessel elements.

Causes of carotid artery dissection include the following:

The annual incidence of symptomatic spontaneous internal carotid artery dissection is 2.5-3 per 100,000. ^[1] The incidence of carotid artery dissection as a result of blunt injuries (mainly high-speed motor vehicle accidents) ranges from less than 1% to 3%. ^[6] The actual incidence may be higher; some dissections are asymptomatic or cause only minor transient symptoms and remain undiagnosed.

Internal carotid artery dissection is a common cause of ischemic stroke in patients younger than 50 years and accounts for as many as 25% of ischemic strokes in young and middle-aged patients. ^[1] The mean age for ischemic stroke secondary to internal carotid artery dissection from blunt traumatic injury is even younger: 35-38 years. Dissection of the intracranial part of the internal carotid artery is rare at any age, because the intracranial carotid artery is less mobile and the skull absorbs most of the force of trauma.

No significant gender-based difference in frequency exists for spontaneous internal carotid artery dissection, though there may be a slight male preponderance when traumatic causes of carotid artery dissection are taken into account.

In general, the prognosis depends on the severity of the initial ischemic injury and the extent of collateral circulation. Overall, the prognosis for spontaneous internal carotid artery dissection is favorable, with about 75% of patients making a good recovery. ^{[1, 7]} The reported mortality is less than 5%. Patients who have a dissection secondary to trauma have a much higher mortality on discharge.

Morbidity from carotid artery dissection ranges in severity from transient focal deficits to permanent cerebral or retinal ischemic injury. More than one half of patients with spontaneous carotid artery dissection develop stroke, ^[1]  though this may be delayed by hours or days. Rates of delayed stroke due to blunt-traumatic causes of carotid artery injury range from 3% in grade I injuries to 44% in grade IV injuries. ^[2]

In the setting of blunt trauma, 37-58% of patients have permanent neurologic deficits on discharge, ^[6] though early use of antithrombotic therapy has essentially eliminated ischemic events in asymptomatic patients with carotid artery dissection. ^{[4, 8]}

As with other causes of stroke in young adults, the functional outcome is generally good, and recurrence of cerebral ischemia and carotid artery dissection is rare. ^[5] The risk of recurrence is highest in the first month and then remains in the area of 1% per year for about a decade. Headache may persist, in some cases for years after the dissection.

Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med. 2001 Mar 22. 344(12):898-906. [Medline].

Redekop GJ. Extracranial carotid and vertebral artery dissection: a review. Can J Neurol Sci. 2008 May. 35(2):146-52. [Medline].

Goyal MS, Derdeyn CP. The diagnosis and management of supraaortic arterial dissections. Curr Opin Neurol. 2009 Feb. 22(1):80-9. [Medline].

Cothren CC, Moore EE, Biffl WL, Ciesla DJ, Ray CE Jr, Johnson JL. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg. 2004 May. 139(5):540-5; discussion 545-6. [Medline].

Debette S, Leys D. Cervical-artery dissections: predisposing factors, diagnosis, and outcome. Lancet Neurol. 2009 Jul. 8(7):668-78. [Medline].

Baker WE, Wassermann J. Unsuspected vascular trauma: blunt arterial injuries. Emerg Med Clin North Am. 2004 Nov. 22(4):1081-98. [Medline].

Baumgartner RW. Management of spontaneous dissection of the cervical carotid artery. Acta Neurochir Suppl. 2010. 107:57-61. [Medline].

Arthurs ZM, Starnes BW. Blunt carotid and vertebral artery injuries. Injury. 2008 Nov. 39(11):1232-41. [Medline].

Tobin J, Flitman S. Cluster-like headaches associated with internal carotid artery dissection responsive to verapamil. Headache. 2008 Mar. 48(3):461-6. [Medline].

Divjak I, Slankamenac P, Jovicevic M, Zikic TR, Prokin AL, Jovanovic A. A case series of 22 patients with internal carotid artery dissection. Med Pregl. 2011 Nov-Dec. 64(11-12):575-8. [Medline].

Patel RR, Adam R, Maldjian C, Lincoln CM, Yuen A, Arneja A. Cervical carotid artery dissection: current review of diagnosis and treatment. Cardiol Rev. 2012 May-Jun. 20(3):145-52. [Medline].

Flis CM, Jager HR, Sidhu PS. Carotid and vertebral artery dissections: clinical aspects, imaging features and endovascular treatment. Eur Radiol. 2007 Mar. 17(3):820-34. [Medline].

Caplan LR. Dissections of brain-supplying arteries. Nat Clin Pract Neurol. 2008 Jan. 4(1):34-42. [Medline].

Kim YK, Schulman S. Cervical artery dissection: pathology, epidemiology and management. Thromb Res. 2009 Apr. 123(6):810-21. [Medline].

Stallmeyer MJ, Morales RE, Flanders AE. Imaging of traumatic neurovascular injury. Radiol Clin North Am. 2006 Jan. 44(1):13-39, vii. [Medline].

Arnold M, Baumgartner RW, Stapf C, Nedeltchev K, Buffon F, Benninger D. Ultrasound diagnosis of spontaneous carotid dissection with isolated Horner syndrome. Stroke. 2008 Jan. 39(1):82-6. [Medline].

Heldner MR, Nedelcheva M, Yan X, et al. Dynamic changes of intramural hematoma in patients with acute spontaneous internal carotid artery dissection. Int J Stroke. 2015 Aug. 10(6):887-92. [Medline].

Xianjun H, Zhiming Z. A systematic review of endovascular management of internal carotid artery dissections. Interv Neurol. 2013 Sep. 1(3-4):164-70. [Medline]. [Full Text].

Fava M, Meneses L, Loyola S, Tevah J, Bertoni H, Huete I. Carotid artery dissection: endovascular treatment. Report of 12 patients. Catheter Cardiovasc Interv. 2008 Apr 1. 71(5):694-700. [Medline].

Zhou Y, Yang PF, Hong B, et al. Stent placement for the treatment of complex internal carotid bifurcation aneurysms: a review of 16 cases. Turk Neurosurg. 2013. 23(2):232-40. [Medline].

Juszkat R, Liebert W, Stanisławska K, et al. Extracranial internal carotid artery dissection treated with self-expandable stents: a single-centre experience. Cardiovasc Intervent Radiol. 2015 Dec. 38(6):1451-7. [Medline].

Donnelly A, Sinnott B, Boyle R, Rennie I. Beware the middle-aged migraine: internal carotid artery dissection mimicking migraine in the emergency department. BMJ Case Rep. 2017 Nov 28. 2017:[Medline].

Esianor BI, Haider AS, Engelhardt MI, et al. Intracranial ischemic infarct due to blunt force trauma in a high school football player. Cureus. 2017 Sep 7. 9(9):e1659. [Medline].

David Zohrabian, MD, FAAEM, FACEP Emergency Physician, Emergent Medical Associates, Valley Presbyterian Hospital

David Zohrabian, MD, FAAEM, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine, Emergency Medicine Residents’ Association

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Sanz Laniado Medical Center, Netanya, Israel

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, New York Academy of Medicine, New York Academy of Sciences, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

A Antoine Kazzi MD, Deputy Chief of Staff, American University of Beirut Medical Center; Associate Professor, Department of Emergency Medicine, American University of Beirut, Lebanon

A Antoine Kazzi is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Joseph J Sachter, MD, FACEP Consulting Staff, Department of Emergency Medicine, Muhlenberg Regional Medical Center

Joseph J Sachter, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Carotid Artery Dissection

Research & References of Carotid Artery Dissection|A&C Accounting And Tax Services
Source

Share on Facebook

Tweet

Follow us